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    ABSTRACT: Aims: We evaluated the safety, feasibility and initial effects of therapy with muscle-derived cells (MDCs) for women with stress urinary incontinence (SUI). Methods: MDCs were isolated from an upper-arm muscle biopsy from 16 women with SUI. Cells were isolated by enzymatic digestion and expanded in vitro for 8-10 weeks. A quantity of 0.6-25 × 10(6) of the obtained cells were injected transurethrally into the urethral rhabdosphincter of women under local anesthesia. The cells were placed circumferentially at the 9, 12, and 3 O'clock positions with endoscopic guidance. Results: The initial results of the treatment of SUI with adult muscle-derived stem cells demonstrate the safety and feasibility of using these cells. The 2-year follow-up revealed a 75% success rate, with some patients achieving complete improvement (50%) and some patients achieving partial improvement (25%), suggesting that the prospects for this method are encouraging. Conclusions: Stem cell therapy promises to become a minimally invasive method for the regeneration of the urethral rhabdosphincter muscle. Injecting a small number of cells does not preclude obtaining the desired therapeutic result.
    Neurourology and Urodynamics 03/2014; DOI:10.1002/nau.22404

  • Biomarkers in Medicine 01/2014; 8(1):81-3. DOI:10.2217/bmm.13.119
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    ABSTRACT: Chronic anticoagulation is a standard of care in idiopathic pulmonary arterial hypertension (IPAH). However, hemostatic abnormalities in this disease remain poorly understood. Therefore, we aimed to study markers of thrombogenesis and fibrinolysis in patients with IPAH. We studied 27 consecutive patients (67% female) with IPAH aged 50.0 years (IQR: 41.0 - 65.0) and 16 controls without pulmonary hypertension. Prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin (TAT) complexes were measured to assess thrombogenesis; tissue-type plasminogen activator (tPA) antigen and plasmin-anti-plasmin complex to characterize activation of fibrinolysis; plasminogen activator inhibitor 1 (PAI-1) to measure inhibition of fibrinolysis; and endothelin-1 (ET-1) and interleukin-6 (IL-6) to assess endothelial activation and systemic inflammation, respectively. In addition, in treatment-naive IPAH patients these markers were assessed after 3 months of PAH-specific therapies. TPA (10.1[6.8-15.8] vs 5.2[3.3-7.3] ng/ml, p<0.001), plasmin-anti-plasmin (91.5[60.3-94.2] vs 55.8[51.1-64.9] ng/ml, p<0.001), IL-6 (4.9[2.5-7.9] vs 2.1[1.3-3.8] pg/ml, p=0.001) and ET-1 (3.7 [3.3-4.5] vs 3.4[3.1-3.5], p= 0.03) were higher in patients with IPAH than in controls. In IPAH patients plasmin-anti-plasmin and tPA correlated positively with IL-6 (r=0.39, p=0.04 and r=0.63, p<0.001, respectively) and ET-1 (r=0.55, p=0.003 and r=0.59, p=0.001, respectively). No correlation was found between tPA or plasmin-anti-plasmin and markers of thrombogenesis. Plasmin-anti-plasmin decreased after 3 months of PAH specific therapy while the other markers remained unchanged. In the present study we showed that markers of fibrynolysis were elevated in patients with IPAH however we did not find a clear evidence for increased thrombogenesis in this group of patients. Fibrinolysis, inflammation, and endothelial activation were closely interrelated in IPAH.
    PLoS ONE 12/2013; 8(12):e82628. DOI:10.1371/journal.pone.0082628


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